Previous research has indicated that rats readily self-administer drugs of abuse such as morphine or cocaine (Belleville, 1964; Numan et al., 1975). They also traverse a runway faster for an injection of morphine than for saline or for the aversive, illness-inducing agent, LiCI (White et al., 1977). Despite such evidence that drugs of abuse are reinforcing, rats also avoid intake of a saccharin conditioned stimulus (CS) when paired with a drug of abuse (Le Magnen et al., 1969). Grigson (1997) has suggested that this behavior is mediated by the same properties that support self-administration of the drug. According to the reward comparison hypothesis, rats suppress intake of the saccharin CS because the rewarding properties of the saccharin CS pale in comparison to those of the drugs of abuse. Support for this hypothesis has been provided (Grigson et al., 2000; 2001; 2002) and, if correct, will serve as a model for both cue-induced craving and drug-induced devaluation of natural rewards. Therefore, Specific Aim I will determine whether bilateral ibotenic acid lesions of the gustatory cortex disrupt contrast induced by morphine, cocaine, and sucrose, but not LiCI. Specific Aim II will use a runway and operant chambers to test whether the lesion impairs the establishment of the taste-drug association, responding for the rewarding properties of the drug, and/or drug-seeking behavior following a period of abstinence. Finally, Specific Aim III will determine whether an intact gustatory cortex is essential for retention of a preoperatively acquired association between the saccharin CS and the drug.